L-3,4-dihydroxyphenylalanine (L-DOPA), a precursor of catecholamines, has been believed to be a pharmacologically inert amino acid. We previously showed that depressor and bradycardic responses to L-DOPA-microinjected into the nucleus tractus solitarii (NTS) were suppressed by shRNA knockdown of GPR143. The specific binding of [3H]-L-DOPA was detected in CHO cells expressing GPR143, which was displaced by L-DOPA CHE, an antagonist of L-DOPA. These findings suggest that L-DOPA itself can exert some of its actions through GPR143. GPR143 is expressed in both neuronal and non-neuronal organs including kidney. Although we reported that L-DOPA sensitize the vascular alpha 1 adrenergic receptor through activation of GPR143, peripheral functions of GPR143 are largely unknown. Here we focused on roles of GPR143 in adenine-induced chronic kidney disease model. Gpr143 gene-deficient mice (GPR143-KO) and control mice were fed diets supplemented with 0.2% adenine. Although blood urea nitrogen and serum creatinine levels were similar, Gpr143-KO showed significant body weight loss of adenine diet than did wild type animals. Serum amyloid A gene expression was higher in Gpr143-KO of adenine diet, thereby suggesting that GPR143 may be involved in inflammation.